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A Chronic Sleep Fragmentation Model using Vibrating Orbital Rotor to Induce Cognitive Deficit and Anxiety-Like Behavior in Young Wild-Type Mice
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Prefrontal network dysfunctions in rapid eye movement sleep behavior disorder.

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Resting-state functional connectivity MRI reveals early brain network changes in REM sleep behavior disorder (RBD), a potential biomarker for alpha-synucleinopathies. Abnormalities in executive control and motor networks, but not default mode networks, were observed.

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Area of Science:

  • Neuroimaging
  • Neurology
  • Sleep Medicine

Background:

  • Rapid eye movement sleep behavior disorder (RBD) may indicate early alpha-synucleinopathy.
  • Resting-state functional connectivity magnetic resonance imaging (rsfcMRI) shows promise as an early biomarker.
  • Limited research has explored cognitive networks in RBD using rsfcMRI.

Purpose of the Study:

  • To investigate brain network alterations in patients with RBD using rsfcMRI.
  • To identify potential early biomarkers for alpha-synucleinopathy within cognitive and motor networks.

Main Methods:

  • rsfcMRI data analyzed from 50 RBD patients and 70 healthy controls (HCs).
  • Group independent component analysis identified executive-control (ECN), default-mode (DMN), basal ganglia (BGN), and sensory-motor (SMN) networks.
  • Dual regression analysis compared functional connectivity (FC) between groups; correlation analysis linked FC with clinical/cognitive scales.

Main Results:

  • RBD patients exhibited reduced striatal-prefrontal FC in the ECN, correlating with executive dysfunction.
  • No significant abnormalities were detected in the DMN.
  • Reduced midbrain-pallidum FC in BGN and decreased motor/somatosensory cortex FC in SMN were observed.

Conclusions:

  • Abnormal ECN function may signify cognitive deficits in early alpha-synucleinopathies.
  • Replicated abnormalities in BGN and SMN align with subclinical motor impairments in RBD.
  • RsfcMRI is a potential early biomarker for both cognitive and motor network dysfunction in alpha-synucleinopathies.